Keratitis for UG

Keratitis for UG - BACTERIAL KERATITIS Dr Sanjay...

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Unformatted text preview: BACTERIAL KERATITIS Dr. Sanjay Shrivastava Professor of Ophthalmology Regional Institute of Ophthalmology Gandhi Medical College Bhopal (M.P.) [email protected] Copy of Power point presentation Copy of Power point presentation of Lecture taken for Junior Final Year students of Gandhi Medical College Bhopal Cornea Cornea Anatomical facts The anterior 1/6th transparent avascular structure covered anteriorly by tear film and exposed to external environment . The posterior surface is in contact with aqueous humour. Corneal epithelium is continuous The junction of cornea and sclera is represented by highly vascularized limbus which contains stem cells which serves as reservoir of pluripotential cells Anatomical facts Anatomical facts Measurements of adult cornea Horizontal Vertical Thickness : 11 ­12 mm : 9­11 mm : central : peripheral 0.5 mm 0.7 – 1 mm Optical properties of Cornea Dependant on Transparency Smoothness of surface Contour Refractive index • Refractive power of Cornea is 40 – 44 Diopter (i.e. 2/3rd of total refractive power of eye) Maintenance of corneal integrity Maintenance of normal corneal integrity 1. Role of environmental (Chemical/ biological agents/physical events of outside world affect integrity) 2. Epithelial maintenance: limbal stem cells and basal cells are capable of proliferation Maintenance of corneal integrity Maintenance of corneal integrity 3. Epithelial movement: intracellular signal, transduction, fibronectine integrin system, proteolytic enzymes, hyaluronin and growth factor play an important role in wound healing 4. Neural regulation 5. Stromal maintenance Introduction Introduction Microbial Keratitis is defined as infectious Corneal ulcer due to proliferation of microorganisms (including bacteria, fungi, viruses and parasites) associated with inflammation and corneal tissue destruction. It is potentially sight threatening condition and should be considered as ocular emergency. Bacterial Keratitis Bacterial Keratitis is most common cause of suppurative corneal ulceration. There are no specific clinical signs to help confirm a definite bacterial cause in Bacterial Keratitis. Identification of risk factors and assessment of the distinctive corneal findings will help in determination of potential etiologies. Host Defense and Risk Factors Host Defense and Risk Factors Defense of Ocular Surface Defense of Ocular Surface Normal Defense mechanisms: 1. Eyelids 2. Tear film proteins (Secretory immunoglobulins, complement components, and various enzymes including lysozyme, lactoferrin, betalysins, orosomucoid and ceruloplasmin have antibacterial effect) 3. Corneal epithelium 4. Normal ocular flora 5. Conjunctival mucosal associated lymphoid tissue (MALT) which is present in subepithelium Risk Factors 1. 2. 3. 4. Compromised normal ocular surface Chronic colonization and infection of the eyelid margin and lacrimal outflow system can predispose cornea Chronic epiphora by reducing concentration of certain antibacterial substances. Dry eye Risk Factors Risk Factors 5. Presence of N Gonorrhoeae, C Diphtheriae, Hemophilus Aegyptius and Listeria Monocytogenes – they can penetrate intact corneal epithelium. 6. Compromised corneal epithelium as in cases of contact lenses users, corneal trauma, corneal surgery bullous keratopathy. 7. Absence of normal conjunctival flora. Risk Factors 8 Biofilm­ is a slimy layer composed of organic polymers produced by embedded bacteria on contact lens, it protects bacteria from antibacterial substances and provide a nidus for infection. 9. Corneal anaesthesia 10. Abuse of topical anaesthetic solution Risk Factors 11. Local immune suppression as due to topical corticosteroids 12. Previous viral infection 13. Drugs used in viral keratitis 14. Corneal hypesthesia External Risk Factors Trauma (Nocardia) 2. Exposure to contaminated water or solutions 3. Chronic abuse of topical anaesthetic solution 4. Crack Cocaine smoking (disrupting corneal epithelium via associated cellular and neuronal toxicity. 1. Predisposing Systemic Conditions Predisposing Systemic Conditions Malnutrition 2. Diabetes 3. Collagen vascular diseases 4. Chronic alcoholism 1. Etiological Factors Inflammation of Cornea (Keratitis) may develop as a result of: 1. Exogenous infection – Mostly traumatic, the object causing injury may carry infection to cornea or may come from conjunctival sac (infecting abraded cornea) 2. Endogenous Infection (inflammation): this is immunological in nature eg. Phlyctenular keratitis caused by tubercular or staphylococcal hypersensitivity and interstitial keratitis related to measles or syphilis. These conditions are commonly noticed at corneal margin (Marginal Keratitis or Marginal Corneal Ulcer) Etiological Factors 3. Spread of Infection from neighboring structures due to anatomical continuity. From conjunctiva to corneal epithelium (eg. Trachoma and Vernal Keratoconjunctivitis) From Sclera to corneal stroma (eg. Sclerosing Keratitis) and From Uveal tract to corneal endothelium (eg. Herpetic Uveitis causing endothelitis) Classification I. II. According to location: a. Superficial b. Deep According to Etiology a. Infective b. Immune mediated c. Traumatic d. Neoplastic e. Degenerative Bacterial Keratitis Bacterial Keratitis Two forms: 1. Central Keratitis 2. Peripheral Keratitis. Corneal Ulcer Superficial Purulent Keratitis (Bacterial Corneal Ulcer) Caused by organisms which produce toxins causing tissue death i.e. necrosis characterised by pus formation. Such purulent keratitis is usually exogenous due to infection by pyogenic bacteria such as pseudomonas, staphylococcus aureus and albus, pneumococcus, N. gonorrhoeae and C. diphtheriae Corneal Ulcer Corneal Ulcer Presence of N Gonorrhoeae, C Diphtheriae, Hemophilus Aegyptius and Listeria Monocytogenes – they can penetrate intact corneal epithelium. Otherwise most of the bacteria including Pneumococcus is capable of producing corneal ulcer when epithelium is damaged Pathogenesis Steps 1. Corneal abrasion 2. Infection by microorganism in presence of predisposing factor(s). The predisposing factors are trauma, long term use of steroids, misdirected eye lashes, mal­apposition of lids, entropion, lagophthalmos, contact lens wear, bullous keratopathy, poor hygienic condition, malnutrition, ocular surface disorders, vitamin A deficiency, causing corneal necrosis (Keratomalacia), corneal edema and trigeminal nerve paralysis (Neurotropic keratitis) Pathogenesis 3. Localized necrosis of superficial layers of cornea 4. Formation of sequestrum with disintegration. It cast off in conjunctival sac 5. Desquamation of corneal epithelium and damage to Bowman’s membrane (area of epithelial and Bowman’s denudation is larger than ulcer) Pathogenesis 6. Epithelial regeneration, at times it covers the edges and floor area 7. A saucer shaped defect with projecting walls above the normal surface due to swelling of tissue resulting from fluid imbibition by corneal stroma 8. Surrounding area is packed by leucocytes, seen as gray zone of infiltration. This is progressive stage. Pathogenesis 9. Necrotic material fall off­ ulcer becomes larger −> infiltration and swelling reduce and disappears −> margin becomes −> margin becomes smooth, floor also looks smooth and transparent. This is regressive stage. 10. Vascularization develops from limus to corneal ulcer to restore lost tissue and to supply antibodies. Pathogenesis 11. Vascularisation is followed by cicatrization due to regeneration of collagen and formation of fibrous tissue 12. Newly formed fibres are laid down irregularly, not conforming to normal pattern of stromal fibres. Therefore this fibrous tissue reflects light irregularly. The scar tissue is more or less opaque. Some vessels may persist in large scar Pathogenesis 13. Bowman’s membrane never regenerates and whenever it is destroyed some degree of corneal opacity remains 14 Corneal opacity may clear with time especially if it is not dense. The vascularization plays part in clearing corneal opacity 15. The scar tissue usually fill the gap exactly, but some deficiency may remain giving rise to formation of corneal facet. The corneal facet may be transparent and may be associated with marked diminution of vision Pathogenesis 16. Diffusion of bacterial toxins into the anterior chamber leads to hyperaemia and inflammation of the iris and ciliary body (Keratouveitis). Polymorphonuclear cells coming out from the uveal tissue may gravitate to bottom of anterior chamber to form hypopyon. Symptoms of Corneal Ulcer Symptoms are usually marked, they are: 1. Diminution of vision, depending on location of corneal ulcer 2. Watering (lacrimation) 3. Difficulty in opening eyes especially in bright light (photophobia and blepharospasm) 4. Pain and foreign body/ gritty sensation 5. There may be discharge (Mucopurulent / purulent) Presentation Clinical signs and symptoms are variable dependent on the virulence of the organism, duration of infection, pre­ existing corneal conditions, immune status of host and previous use of antibiotics/ steroid Acanthamoeba can cause masquerading syndrome mimicking bacterial keratitis. Signs 1. 2. 3. 4. 5. Visual acuity may be affected, depending on location of corneal ulcer Edema of lids of affected eye, in severe cases Blepharospasm Ciliary and conjunctival congestion Hazyness / pus may be present in anterior chamber Signs 6. Colour and pattern of iris may be disturbed 7. Cornea: loss of transparency the ulcer appears yellowish/ grayish pale lesion of varying shape /size, breach in continuity of corneal surface, ulcer with irregular floor and margins, floor appears grayish / grayish pale/ grayish yellow, zone of infiltration with projecting swollen edges. The surrounding cornea may appear ground glass like due to corneal edema Corneal Ulcer Corneal Ulcer Peripheral Corneal Ulcer Central Corneal ulcer involving Lower periphery also Clinical Examination Evaluation of predisposing and aggravating Factors 1. A detailed history 2. Prior ocular history 3. Review of related medical problems, current ocular medications and history of medication allergy Examination Visual acuity 2. An external ocular examination Facial appearance, eyelids, lid closure Conjunctiva, Nasolacrimal apparatus, corneal sensation 1. Examination 3. Slit Lamp Biomicroscopy: For Eyelid margin Tear film Conjunctiva Sclera Cornea (epithelial defects, punctate keratopathy, edema, stromal infiltrates/ulceration, thinning or perforation) Slit Lamp Examination… Contd Slit Lamp Examination… Contd Location of lesion Density, Size , shape , depth, colour Endothelium Anterior chamber Loose or Broken sutures Signs of corneal dystrophy Signs of previous inflammation Slit Lamp Examination… Contd Anterior Vitreous Fluorescein Rose Bengal staining Differential Diagnosis Differential Diagnosis Differentiate from Non­infectious causes of infiltrates 1. Fungal 2. Protozoal 3. Nematodes 4. Viral infections, HSV, VZV, EBV 5. Contact lens infiltrates 6. Collagen Vascular Diseases Differential Diagnosis 7. Sarcoidosis 8. Severe Rosacea 9. Allergic Conditions 10. Corneal Trauma , FB and Loose sutures Complications of Corneal Ulcer Spread of ulcer horizontally and depth­ wise, leading to thinning of cornea 2. Bulging of descemet’s membrane (Keratocele or Descemetocele). This appears as transparent vesicle surrounded by grayish zone of infiltration. Bulging of descemet’s membrane represents condition of impending perforation of cornea 1. Complications of Corneal Ulcer Complications of Corneal Ulcer 3. Perforation of ulcer is generally caused by sudden exertion such as coughing, sneezing, straining at stool or firm closure of eyes. Exertion causes rise of blood pressure and results in increase in intra­ ocular pressure (IOP). Weak area of ulcer is unable to support the increased IOP , gives way and perforation develops Complications of Corneal Ulcer Complications of Corneal Ulcer PERFORATION OF CORNEAL ULCER Complications of perforation may be serious and sight threatening A. Peripheral perforation: Iris is thrown forward −> opening is occluded −> −> anterior chamber is formed , scarring takes place: takes a. Iris may be pushed back to normal position or Complications of Corneal Ulcer Complications of Corneal Ulcer b. Iris may remains adherent to corneal scar (anterior synechia) If peripheral perforation is large the pupillary border of iris prolapse through opening. Exudation takes place on prolapsed tissue −> an adherent leucoma forms (it may be flat or bulging) Complications of Corneal Ulcer B. Central perforation: small central perforation −> anterior chamber collapse −> −> lens comes in contact with corneal endothelial surface −> anterior capsular cataract −> repeated healing and perforation leading to corneal fistula formation Complications of Corneal Ulcer Complications of Corneal Ulcer C. Sloughing of whole cornea: prolapse of iris −> pupillary block and exudation on iris −> pseudocornea formation (iris covered with exudates , formation of fibrous tissue and formation of scar tissue) −> anterior chamber anatomy is lost , angle of anterior chamber is occluded leading to secondary glaucoma −> anterior staphyloma (an ectatic cicatric with incarceration of iris). Anterior staphyloma may be partial or total. Complications of Corneal Ulcer In case of sudden large perforation lens may subluxate or thrown out due to rupture of suspensory ligaments. Lens and vitreous may prolapse through perforation. Intraocular haemorrhage may occur due to dilatation and rupture of intra­ocular blood vessels due to sudden hypotony. This may lead to vitreous haemorrhage , choroidal , sub­retinal or sub­ choroidal haemorrhage. In elderly patients there may be expulsive haemorrhage Complications of Corneal Ulcer D. Intra­ocular purulent infection: due to perforation bacteria enter in the eye and causes purulent iridocyclitis, endophthalmitis and panophthalmitis Treatment of uncomplicated corneal ulcer Treatment of uncomplicated corneal ulcer LOCAL TREATMENT 1. Control of infection with appropriate antibiotic(s) a. based on clinical judgment b. based on finding of smear examination c. based on culture and sensitivity report Local Antibiotic therapy Local Antibiotic therapy Antibiotic drops frequently, ointment may be used at bedtime in less severe cases. Collagen shield or soft contact lenses soaked in antibiotics are sometimes used and may enhance drug delivery. Sub­conjunctival antibiotics may be helpful where there is imminent scleral spread or perforation or in cases where compliance with the treatment regimen is questionable Therapeutic Agents Therapeutic Agents No organism identified or multiple types of organisms Cefazolin: Topical – 50 mgm/ml; S/c 100 mgm in 0.5 ml. With Tobramycin / Gentamicin: Topical – 9­14 mgm/ml; S/c 20 mgm in 0.5 ml. Fluroquinolones: 3 mgm/ ml 1. Therapeutic Agents Therapeutic Agents 2. Gram Positive Cocci Cefazolin: Topical – 50 mgm/ml; S/c 100 mgm in 0.5 ml. Vancomycin: Topical –15 ­ 50 mgm/ml; S/c 25 mgm in 0.5 ml. Gram Negative Rods Gram Negative Rods Tobramycin / Gentamicin: Topical – 9­14 mgm/ml; S/c 20 mgm in 0.5 ml. Ceftazidime : Topical – 50 mgm/ml; S/c 100mgm in 0.5 ml. Fluroquinolones: 3 mgm/ ml Gram Negative Cocci Gram Negative Cocci Ceftriaxone : Topical – 50 mgm/ml; S/c 100 mgm in 0.5 ml. Ceftazidime : Topical – 50 mgm/ml; S/c 100 mgm in 0.5 ml. Fluroquinolones: 3 mgm/ ml Treatment of uncomplicated corneal ulcer Treatment of uncomplicated corneal ulcer 2. Cycloplegic and mydriatic drug: atropine 1% or cyclopentolate 1% or Homatropine 2%. These drugs prevents ciliary spasm, relieves pain, prevent dangerous results of iridocyclitis, breaks adhesions and prevent synechia formation Treatment of uncomplicated corneal ulcer Treatment of uncomplicated corneal ulcer 3. Cleanliness: Irrigation with luke warm normal saline or 2% luke warm boric acid solution to remove conjunctival discharge and necrotic material 4. Application of heat: provides comfort and causes vasodilatation 5. Protection of eye from external environment with dark glasses Treatment of uncomplicated corneal ulcer Treatment of uncomplicated corneal ulcer Steroids must not be used in presence of active infected corneal ulcer In cases of progressive corneal ulcer despite routine therapeutic treatment, the following measures be considered: Scraping of ulcer floor followed by cauterization with pure (100%) carbolic acid or 10­20% trichloracetic acid. Povidone Iodine can also be used for cauterization Systemic Treatment Systemic Treatment 1. Systemic Antibiotics: consider in sever cases with scleral or intra­ocular extension of infection or with impending or frank perforation of the cornea Systemic antibiotic therapy is necessary in cases of Gonococcal keratitis due to its fulminating nature and systemic involvement Systemic Treatment Systemic Treatment 2. Analgesic anti­inflammatory 3. Supportive treatment 4. Acetazolamide Tab is added in cases of impending perforation or perforated corneal ulcer and in cases where there is raised intra­ocular tension (in dosage of 250 mgm upto four times a day) Non­responsive / Progressive Corneal Ulcer Non­responsive / Progressive Corneal Ulcer TREATMENT Re­evaluate for Drug toxicity Non­infectious causes or Unusual organisms such as non­tubercular mycobacteria, Nocardia or acanthamoeba should be suspected Modification of anti­microbial therapy Therapeutic keratoplasty may be undertaken Indolent / Non­healing Ulcer Indolent / Non­healing Ulcer Consider debridement of necrotic corneal stroma and Frequent lubrication and/or Temporary tarsorrhaphy Treatment of Keratocele or Descemetocele Treatment of Keratocele or Descemetocele Continue use of local antibiotics, atropine, add topical antiglaucoma medication (like Timolol or Betaxolol) or add systemic acetazolamide, bandage contact lens is beneficial. All forced expiration like coughing, sneezing, blowing of nose etc must be avoided Treatment of perforated corneal ulcer Treatment of perforated corneal ulcer Rest Continue treatment of corneal ulcer with modification, i.e. firm bandage or bandage contact lens All forced expiration like coughing, sneezing, blowing of nose etc must be avoided Use of tissue adhesive (Glue): N­butyl 2­ethyl cyanoacrylate Therapeutic penetrating keratoplasty or conjunctival flap Adjunctive Therapy Cyanoacrylate tissue glue 2. Therapeutic Contact Lenses 1. Surgical Treatment Conjunctival flap; In recalcitrant bacterial keratitis 2. Penetrating Keratoplasty (PKP): Large central ulcer , presenting late History of previous ocular surgery Injudicious use steroid treatment 1. ...
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